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However, the specific mechanisms that initiate the fibrotic cascade in endometriosis remain poorly defined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Spatial transcriptomics (ST) and cellular interaction analyses were performed on human specimens of endometriotic lesions and normal endometrium. An endometriosis mouse model was used to evaluate the effect of IL-17\u00a0C neutralization with the MOR106 antibody on ectopic lesion growth and fibrosis. In vitro experiments were conducted to explore the role of IL-17\u00a0C in macrophage polarization and extracellular matrix (ECM) production by endometrial stromal cells (ESCs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>IL-17RE expression was significantly upregulated in endometriotic tissues compared with normal endometrium and correlated with endometriosis fibrosis. IL-17\u00a0C levels were markedly higher in patient-derived tissues and peritoneal fluid. In a mouse model of endometriosis, neutralization of IL-17\u00a0C with the MOR106 antibody inhibited ectopic lesion growth and alleviated fibrosis in both eutopic and ectopic endometrium. Importantly, MOR106 selectively reduced CD206\u2009+\u2009M2 macrophage infiltration in lesions without significantly altering the M1 macrophage population, suggesting that IL-17\u00a0C primarily drives M2-like macrophage accumulation in vivo. In vitro, IL-17\u00a0C promoted macrophage polarization toward a pro-fibrotic M2-like phenotype, and these IL-17\u00a0C-induced M2 macrophages enhanced ECM production by ESCs via activation of the MAPK\/ERK pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Targeting the IL-17\u00a0C\/IL-17RE axis provides a promising novel therapeutic strategy for mitigating fibrosis in endometriosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12967-026-08769-9","type":"journal-article","created":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T16:53:57Z","timestamp":1785948837000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting the IL-17C-M2 macrophage axis ameliorates fibrosis in endometriosis through MAPK\/ERK signaling"],"prefix":"10.1186","volume":"24","author":[{"given":"Jingling","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Yao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liuying","family":"Chu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gendie E.","family":"Lash","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinsheng","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minghua","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xuefeng","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3473-6553","authenticated-orcid":false,"given":"Ping","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,8,5]]},"reference":[{"key":"8769_CR1","doi-asserted-by":"publisher","first-page":"721","DOI":"10.12688\/f1000research.152368.3","volume":"13","author":"MM Anchan","year":"2024","unstructured":"Anchan MM, Kalthur G, Datta R, Majumdar K, Dutta PK. 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